Entire coding region of GluRIIA has been deleted, plus 300bp of 5' flanking sequence and a similar extent of 3' flanking sequence.
Deletion of entire coding region of GluRIIA, plus 300bp of 5' flanking sequence and a similar extent of 3' flanking sequence. The position of the deletion on the reference sequence is approximate and was inferred by the FlyBase curator based on the author statement.
GluRIIAAD9 heterozygous third instar larvae display significant deficit in locomotion (measured as distance crawled per unit of time).
In homozygous GluRIIAAD9 mutants all A-type receptors are absent, whereas B-type receptor clusters are still present in the neuromuscular junction.
Latrunculin A treatment of GluRIIAAD9 mutants has no effect on receptor cluster size or sEJC amplitude (compared to a reduction in wild-type). Similarly, postsynaptic latrunculin has no effect on sEJC amplitude in GluRIIAAD9 mutants.
The mean sEJC amplitude in GluRIIAAD9 mutants is approximately one-half the amplitude of wild-type animals, consistent with complete and specific loss of A-type receptors.
The morphological development of neuromuscular junctions (NMJs) in GluRIIAAD9/Df(2L)cl-h4 mutants is indistinguishable from wild type when larvae are reared at 18 or 25oC. However, when wild-type larvae are raised at 29oC, size-matched animals show consistently larger and more complex NMJs with more boutons. This bouton outgrowth does occur in GluRIIAAD9/Df(2L)cl-h4 mutants reared at 29oC, but to a much lower extent than wild type. At 29oC, GluRIIAAD9/Df(2L)cl-h4 mutants show an increase in stride-frequency that is comparable to wild type, but a lower increase in speed of locomotion and crawling distance than that seen in wild type and no change in stride frequency, which does increase in wild type. The mutants have an altered locomotor pattern to wild-type larvae; they rest more and show only short stretches of uninterrupted movement.
GluRIIAAD9/Df(2L)cl-h4 flies have a postsynaptic defect, which causes a reduction in average quantal size and an increased junctional quantal content. At the larval stage, these mutants develop fewer presynaptic boutons but, as compensation, they have a greater density of T-bars within these boutons compared to wild type. This results in the release of more vesicles per action potential and the production of larger evoked Ca2+ signals. However, there is still a strong depression of postsynaptic responses that saturate at around 60% of the initial enhanced excitatory junctional potential (eEJP) amplitude.
Shows no obvious behavioral phenotype. Heterozygotes with Df(2L)cl-h4 show large decrease in quantal size, as recorded in muscle 6, segment A3 of female third instar larvae. There is no change in evoked release, indicating a compensatory increase in number of vesicles released, i.e. in quantal content. This is confirmed by failure analysis, using reduced external calcium concentrations. There is a small but significant decrease in bouton number on muscles 6 and 7 in the mutant. The up-regulation of transmitter release is observed over a range of calcium concentrations. Short-term facilitation is not altered at 10Hz or 20Hz.
GluRIIAAD9 has abnormal neurophysiology phenotype, suppressible by pAbpk10109
The elimination of one copy of GluRIIA in pAbpk10109/+, GluRIIAAD9/+ mutants results in an almost complete suppression of enhanced junctional signal transmission and in a corresponding suppression of junctional growth, indicating that animals with genetically restricted GluRIIA expression are incapable of developing a strengthened larval stage neuromuscular junction.
Scer\GAL4elav-C155-mediated expression of Avic\GFPCameleon2.0.Scer\UAS does not affect the neurological phenotype of GluRIIAAD9 mutants.
